Lipid Guidelines - Dr. Ajay Kantharia

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Lipids are a heterogenous group of …

Lipids are a heterogenous group of
water –insoluble ( hydrophobic ) organic
molecules. Presentation on how they affect the body and what to do to prevent their effects.

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  • 2-4 gms EPA + DHA Is only in case of elevated triglycerides above 150 mg/ dl. But for the rest of the public it is 1 g/ day. Quoted below -
    'In the US, the American Heart Association (AHA) recommends the general public consume 2 fatty fish per week; while those with documented heart disease should consume 1 gram of long chain omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) per day via diet or supplementation. '
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  • thanks your slide,, is very good information for me, but how am I can down load in PPT ( power point)
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  • Other dietary considerations include to limit trans fatty foods . Diets that lower cholesterol include plant stanols/sterols (2 g/day) and soluble fiber (10-25 g/day). The role of alcohol is not well-defined.
  • The role and benefits of exercise is to be stressed: Aerobic exercise of > 20 minutes per activity for at least 3 days per week has been proved to be beneficial. Exercise also promotes weight loss and  HDL
  • Complete cessation of smoking c an lower oxidative stress, reverses endothelial dysfunction and  HDL.
  • Weight loss by exercise and dieting increases HDL, i mproves glycemic control and reduces blood pressure
  • Cholesterol lowering drug therapy includes : HMG CoA Reductase Inhibitors: Lovastatin,Pravastatin,Simvastatin,Fluvastatin,Atorvastatin and Rosuvastatin Cholesterol Absorption Inhibitors: Ezetimibe Fibrates: Gemfibrozil,Micronized Fenofibrate and Clofibrate Bile Acid Sequestrants: Cholestyramine ,Colestipol and Colesevelam And Niacin
  • HMG CoA reductase acts directly on the cholesterol and bile acids .
  • Dosage of statins depends on the level of LDL : Start with lower dose and increase as needed . Doses should be given in the evening or at bedtime (Atorva and Rosuva can be given any time) . May need to decrease dose occasionally by adding potentially interacting drug if a profound drop in LDL is noted.
  • Side effects of statins include : Major toxicitieslike  Hepatic transaminases , myalgias and rhabdomyolysis . Selected minor adverse effects like d yspepsia/heartburn , headache and taste disturbances
  • Monitoring of the drug therapy must be done at regular intervals : Lipid Profiles Before initiation and at 6-12 weeks until stable Every 6 months thereafter Hepatic Transaminases Baseline and every 6-12 weeks until stable Every 6 months thereafter Creatine Kinase (CK) Only as needed Glucose and Uric Acid .
  • Signs and symptoms of myotoxicity include : Symptoms consist primarily of gradually decreased muscle strength and localized or generalized muscle weakness. Symptoms can occur within days or may not occur for years after starting therapy. Symptoms involving other organ systems (such as fatigue, shortness of breath, decreased urine output, dark-colored/turbid urine).
  • Graph shows the comparative LDL lowering effects of statins .
  • Graph shows a comparative study of statins and the beneficial effects on the HDL levels
  • Graph shows comparison of statins and their effect on lowering of TG levels
  • Drug interactions of statins include risk of hepatotoxicity and/or myalgias or myopathy when combined with fibrates or niacin Statins  absorption with bile acid sequestrants, inhibit or induce CYP-based metabolism and inhibit CYP activity
  • Mechanism of action of fibrates include :Inhibition of cholesterol synthesis, decreased TG synthesis, inhibition of lipolysis in adipose tissue, decreased production of VLDL/  clearance and increased plasma and hepatic LPL activity. Effect on lipids includes  TC,  LDL,  HDLand  TG .
  • Dosing of fibrates are : Gemfibrozil: 600mg BID Micronized Fenofibrate: 67mg QD;  to 67-201mg QD Clofibrate: 2g daily in divided doses Adverse effects are Nausea, diarrhea, cholelithiasis, phototoxicity Drug interactions include Increased risk of hepatotoxicity and/or myalgias with concurrent statins and/or niacin and protein binding displacement (e.g., warfarin
  • Niacin: The Mechanism of action includes inhibition of free fatty acid release from adipose tissue,inhibition of cAMP accumulation ,inhibition of VLDL and LDL synthesis and increased LPL activity. The effects on lipids are that it  TC,  LDL,  HDL,  TG , c onverts LDL phenotypic pattern B into pattern A and lowers Lp(a) .
  • Niacin is immediately released in dose of 100mg TID; it may be  by 100mg TID every week as tolerated and the ideal goal = 500-1000mg TID . Sustained release tablets are also available as 375mg QD; it maybe  gradually as needed to an ideal goal = 500-2000mg QD.
  • Precautions while adminstering niacin to be kept in mind are the adverse effects that include f lushing, pruritis, headache, fatigue (PG-mediated? -- ASA), gastritis, abdominal pain, aggravation of PUD, hepatotoxicity ,impaired glucose control and  uric acid concentrations. The drug interactions include with alcohol:  risk of hepatotoxicity , with Statins, fibrates:  risk of hepatotoxicity and/or myalgias. Contra-Indication are a H/o gout,peptic ulcer disease, liver disease.
  • Bile acids reaches the gut and bile acid sequestrants prevent re-entry into the liver.
  • Ezetimibe is the first member of a new class of lipid-lowering drugs that target intestinal absorption by inhibiting absorption of dietary and biliary cholesterol across the intestinal wall. Ezetimibe, co-administered with a statin, at any dose, provides even greater plasma cholesterol reduction by controlling two sources of cholesterol through Dual Inhibition. Ezetimibe may also be useful as monotherapy in patients who cannot tolerate or do not respond to statins. Current data from controlled clinical trials indicate that ezetimibe has a favorable safety profile, alone it is similar to placebo and when co-administered with a statin, similar to the statin alone. Co-administration therapy with a statin and ezetimibe should decrease the need for statin dose adjustments, broaden lipid control, and facilitate achievement and maintenance of LDL-C goals.
  • Ezetimibe is useful as monotherapy for patients intolerant or nonresponsive to statins or enhanced benefits in addition to statins. Favorable safety and tolerability profile shown in clinical trials reveal they are similar to placebo, similar to statin alone, in coadministration
  • Certain herbs and natural products are found to be beneficial : Garlic Fish Oils Red Yeast Rice Dietary Fiber Oat Bran Plant Sterols Guggul CoEnzyme Q10

Transcript

  • 1. Consulting Physician & Cardiologist Critical Care Physician HON. PHYSICIAN : Saifee Hospital Sir H. N. Hospital Motiben Dalvi Hospital Lipids Guidelines
  • 2.
    • The food that we eat is mixture of
      • Carbohydrates
      • Proteins
      • Fats (LIPIDS)
      • Fibres
      • Vitamins, minerals, etc
  • 3. LIPIDS
    • Lipids are a heterogenous group of
    • water –insoluble ( hydrophobic ) organic
    • molecules .
  • 4. Lipids are
    • Major source of energy
    • Other function .
    • Fat soluble vitamins have regulatory or coenzyme function.
    • Prostaglandin & steroid hormones
  • 5. An adult ingests about 60-150 gm of lipids / day. 90% is Triglycerides (TG) The remaining 10% is cholesterol , cholesteryl esters , phospholipids and unesterified (free ) fatty acids.
  • 6.
    • The bowel has limited capacity for the uptake of cholesterol approximately 1500mg/ day,
    • but the uptake of the TG is unlimited .
  • 7.
    • The various lipids are emulsified,
    • degraded, mixed by and with various
    • digestive juices & enzymes so that it can
    • be absorbed.
    • The primary site of lipid absorption is the
    • brush border membrane of the intestinal
    • mucosal cells.
    • From the intestinal mucosal cells they are
    • transported to the lymph >> thoracic duct into
    • the circulation.
  • 8. LIPID PROFILE
    • Total Cholesterol
    • Triglyceride
    • High Density Lipoprotein
    • Low Density Lipoprotein
    • Very Low Density Lipoprotein
    • Chylomicrons
    • Various Ratios
  • 9. What is a Lipoprotein? Protein Lipo (Lipid) + Lipoprotein is a macro-molecular complex in blood carrying protected lipids
  • 10. Why are lipoproteins formed? Cholesterol is insoluble in water To transport it thro’ blood (92% water) it is combined with Protein to make Watersoluble Lipo proteins -Harper’s Biochemistry (2000),p 268 For utilization and storage in tissues,it is converted to water-insoluble Cholesterol ‘Ester’ -Krause’s (2000), Food,Nutrition and Diet Therapy, p 62
  • 11. Structure of a Lipoprotein
  • 12. What is a Apolipoprotein? -Harper’s Biochemistry (2000),p 270 Apo = ‘Derived from’ Apolipoprotein is the name given to ‘ Protein’ part of Lipoprotein (ie,Protein derived from Lipoprotein)
  • 13. APOLIPOPROTEINS
    • Stabilize the Lipoprotein Structure.
    • Important regulatory function in LIPOPROTEIN metabolism.
  • 14. Which Lipoproteins have which Apolipoproteins ? -Harper’s Biochemistry (2000),p 270 Apolipoprotein Lipoprotein Apo A-I/II/IV HDL,Chylo Apo C-I/II/III VLDL,HDL,Chylo Apo D HDL Apo E VLDL,LDL,HDL,Chylo B-100 has the longest amino acidchain(4536) B-48 means 48 % of B 100 Apo B-100 LDL,VLDL,IDL Apo B-48 Chylo
  • 15.
    • Why is the study of Lipid important ?
      • C V D
  • 16. WHOM TO TEST ?
    • A personal history of CHD, peripheral vascular disease or CVA
    • A Family History of CHD or PVD (especially before age 55 years or hyperlipidemia)
    • Hypertension
    • Diabetes mellitus
    • Physical stigmata of hyperlipidermia
    • Obesity (BMI > 28)
    • Chronic Renal Disease
    • Smoking habits
  • 17.
    • When should we start examining
    • Lipid profile ?
  • 18.
    • Adults > 20years of age & then every 05 years
    • Test children with a family history of premature CHD at age 2 years.
  • 19. Frequency of Testing
    • Every 5 years from age 20 – 25 years to 60-70 years according to overall risk.
    • Borderline cases – vary from 1 to 5 years
    • For patients on treatment with Diet – Initially every 3 months then every 6 -12 months
    • For patients on medication – initially every 6 – 8 weeks then every 3-6 months
  • 20. Primary Prevention
    • Primary prevention aims to prevent new onset CHD
  • 21. Primary Prevention and Risk Factor assessment
  • 22. Categories of Risk Factors
    • Major, independent risk factors
    • Life-habit risk factors
    • Emerging risk factors
  • 23. Major Risk Factors (Exclusive of LDL Cholesterol) That Modify LDL Goals
    • Cigarette smoking
    • Hypertension (BP  140/90 mmHg or on antihypertensive medication)
    • Low HDL cholesterol (<40 mg/dL) †
    • Family history of premature CHD
      • CHD in male first degree relative <55 years
      • CHD in female first degree relative <65 years
    • Age (men  45 years; women  55 years)
  • 24. Life-Habit Risk Factors
    • Obesity (BMI  30)
    • Physical inactivity
    • Atherogenic diet
  • 25. Emerging Risk Factors
    • Lipoprotein (a)
    • Homocysteine
    • Prothrombotic factors
    • Proinflammatory factors
    • Impaired fasting glucose
    • Subclinical atherosclerosis
  • 26. Diabetes
    • In ATP III, diabetes is regarded as a CHD risk equivalent.
  • 27. CHD Risk Equivalents
    • Risk for major coronary events equal to that in established CHD
    • 10-year risk for hard CHD >20%
    Hard CHD = myocardial infarction + coronary death
  • 28. CHD Risk Equivalents
    • Other clinical forms of atherosclerotic disease (peripheral arterial disease, abdominal aortic aneurysm, and symptomatic carotid artery disease)
    • Diabetes
    • Multiple risk factors that confer a 10-year risk for CHD >20%
  • 29. ATP III Lipid and Lipoprotein Classification
    • LDL Cholesterol (mg/dL)
    • <100 Optimal
    • 100–129 Near optimal/above optimal
    • 130–159 Borderline high
    • 160–189 High
    •  190 Very high
  • 30. ATP III Lipid and Lipoprotein Classification (continued)
    • HDL Cholesterol (mg/dL)
    • <40 Low
    •  60 High
  • 31. ATP III Lipid and Lipoprotein Classification (continued)
    • Total Cholesterol (mg/dL)
    • <200 Desirable
    • 200–239 Borderline high
    •  240 High
  • 32.  
  • 33.  
  • 34. LDL Cholesterol Goals and Cutpoints for Therapeutic Lifestyle Changes (TLC) and Drug Therapy in Different Risk Categories Risk Category LDL Goal (mg/dL) LDL Level at Which to Initiate Therapeutic Lifestyle Changes (TLC) (mg/dL) LDL Level at Which to Consider Drug Therapy (mg/dL) CHD or CHD Risk Equivalents (10-year risk >20%) <100  100  130 (100–129: drug optional) 2+ Risk Factors (10-year risk  20%) <130  130 10-year risk 10–20%:  130 10-year risk <10%:  160 0–1 Risk Factor <160  160  190 (160–189: LDL-lowering drug optional)
  • 35. And –the latest As per July 13 th 2004 NCEP ATP III update, high risk patient needs to achieve LDL-C<70 mg/dL Risk LDL goal mg/dL(NCEP ATP III) 1 LDL goal (Recommendations for modifications to footnote ATP III) 2 CHD (10 yr risk>20%) < 100 < 70 2+ RF -10 yr risk 10-20% -10 yr risk < 10% < 130 < 130 < 100 Unchanged 0-1 RF < 160 Unchanged
  • 36.  
  • 37. Therapeutic Lifestyle Changes in LDL-Lowering Therapy
    • Major Features
    • TLC Diet
      • Reduced intake of cholesterol-raising nutrients
        • Saturated fats <7% of total calories
        • Dietary cholesterol <200 mg per day
      • LDL-lowering therapeutic options
        • Plant stanols/sterols (2 g per day)
        • Viscous (soluble) fiber (10–25 g per day)
    • Weight reduction
    • Increased physical activity
  • 38. Therapeutic Lifestyle Changes Nutrient Composition of TLC Diet
    • Nutrient Recommended Intake
    • Saturated fat Less than 7% of total calories
    • Polyunsaturated fat Up to 10% of total calories
    • Monounsaturated fat Up to 20% of total calories
    • Total fat 25–35% of total calories
    • Carbohydrate 50–60% of total calories
    • Fiber 20–30 grams per day
    • Protein Approximately 15% of total calories
    • Cholesterol Less than 200 mg/day
    • Total calories (energy) Balance energy intake and expenditure to maintain desirable body weight /prevent weight gain
  • 39. Other Dietary Considerations
    • Limit trans fatty acids
    • Proven dietary components to lower cholesterol:
      • Plant stanols/sterols (2 g/day)
      • Soluble fiber (10-25 g/day)
    • Questionable role of alcohol
  • 40. Exercise
    • Safety
    • Aerobic exercise
      • > 20 minutes per activity
      • At least 3 days per week
    • Promotes weight loss and
    •  HDL
  • 41. Smoking Cessation
    • Can lower oxidative stress
    • Reversal of endothelial dysfunction
    •  HDL
  • 42. Weight Loss
    • Increases HDL
    • Improves glycemic control
    • Reduces blood pressure
  • 43.
    • DRUG THERAPY
  • 44. Drug Therapy
    • The 5 most common clinical situations in
    • which drug therapy is needed are
    • elevated LDL-C;
    • high levels of TGs (200 to 500 mg/dL) despite attainment of LDL-C goals;
    • low HDL-C;
    • diabetic dyslipidemia; and
    • very high TGs and/or chylomicronemia syndrome.
  • 45. Cholesterol-Lowering Drug Therapy
    • HMG CoA Reductase Inhibitors
    • Lovastatin
    • Pravastatin
    • Simvastatin
    • Fluvastatin
    • Atorvastatin
    • Rosuvastatin
    • Cholesterol Absorption
    • Inhibitors
    • Ezetimibe
    • Fibrates
    • Gemfibrozil
    • Micronized Fenofibrate
    • Clofibrate
    • Bile Acid Sequestrants
    • Cholestyramine
    • Colestipol
    • Colesevelam
    • Niacin
  • 46. Statins
    • Statins are the most potent agents for lowering LDL-C. These agents work by
    • competitively inhibiting the rate-limiting step of cholesterol synthesis and
    • upregulating LDL receptors in the liver.
  • 47. HMG CoA Reductase Inhibitors 1.) LDL Uptake Cholesterol 2.) Synthesis HMG CoA Bile Acids Cholesterol HMG CoA Bile Acids
  • 48.
    • Start with lower dose and increase as needed (according to LDL)
      • Pick dose appropriate to LDL-lowering needed
    • Doses should be given in the evening or at bedtime (Atorva and Rosuva can be given any time).
    • May need to decrease dose occasionally
      • Adding potentially interacting drug
      • Profound drop in LDL
    Statins - Dosing
  • 49. Statin Adverse Effects
    • Major toxicities:
    •  Hepatic transaminases
    • Myalgias
    • Rhabdomyolysis
    • Selected minor adverse effects:
    • Dyspepsia/heartburn
    • Headache
    • Taste disturbances
  • 50. Monitoring of Lipid Lowering Therapy
    • Lipid Profiles
      • Before initiation and at 6-12 weeks until stable
      • Every 6 months thereafter
    • Hepatic Transaminases
      • Baseline and every 6-12 weeks until stable
      • Every 6 months thereafter
    • Creatine Kinase (CK)
      • Only as needed
    • Glucose, Uric Acid
  • 51. Signs and Symptoms of Myotoxicity
    • Symptoms consist primarily of gradually decreased muscle strength and localized or generalized muscle weakness.
    • Symptoms can occur within days or may not occur for years after starting therapy.
    • Symptoms involving other organ systems (such as fatigue, shortness of breath, decreased urine output, dark-colored/turbid urine).
  • 52. Comparative LDL Effects -70 -60 -50 -40 -30 -20 -10 0 10 40 20 80 10 10 20 20 20 20 80 40 40 40 40 1 5 20 Atorvastatin Simvastatin Pravastatin Lovastatin Fluvastatin Rosuvastatin Am J Cardiol 1998;81:582-7. Am J Cardiol 2001;88:504-8. J Int Med Res 2000;28:47-68. Clin Cardiol 2000;23:39-46. 80 80 80
  • 53. Comparative HDL Effects -4 -2 0 2 4 6 8 10 12 Atorva Simva Prava Lova Rosuva 10 20 40 40 40 40 20 20 20 20 10 10 40 80 80 Adapted from Jones PH et al. Am J Cardiol 2003;92:152–160 & CURVES Study. Am J Cardiol 1998;81:582-7. 10
  • 54. Comparative TG Effects -35 -30 -25 -20 -15 -10 -5 0 5 10 40 20 80 10 10 20 20 20 20 80 40 40 40 40 Atorvastatin Simvastatin Pravastatin Lovastatin Rosuvaastatin Adapted from Jones PH et al. Am J Cardiol 2003;92:152–160 & CURVES Study. Am J Cardiol 1998;81:582-7. 10
  • 55. Drug Interactions
    • Pharmacodynamic
      • Risk of hepatotoxicity and/or myalgias or myopathy when combined with fibrates or niacin
    • Pharmacokinetic
      •  absorption with bile acid sequestrants
      • Inhibition or induction of CYP-based metabolism
      • Inhibition of CYP activity
  • 56. 2 nd Goal
    • 2 nd Goal after LDL C is TG control :
    • A TG level >150 mg/dL is considered elevated. After correcting LDL- C,
    • TG should be less than 150mg%.
    • For patients with mildly elevated TG values (150 to 199 mg/dL), Diet and exercise may be adequate.
  • 57. 2 nd Goal
    • 2 nd Goal….. TG
            • … ... Non HDL Cholesterol
            • Total Chol. = LDL + VLDL + HDL
            • Non HDL Chol =
            • Total Chol – HDL = LDL + VLDL
  • 58. Non HDL Cholesterol Goal
    • Non HDL Chol Goal =
    • 30 mg above LDL Goal
  • 59. T G
    • Diseases associated with High TG:
    • Type 2 diabetes mellitus,
    • Chronic renal failure, nephritic syndrome, Hypothyroidism,
    • should be looked for and treated.
  • 60. T G
    • Drugs that elevate TGs, such as
    • corticosteroid therapy,
    • estrogen therapy,
    • retinoid therapy, or
    • high doses of beta-blockers,
    • should be stopped or substituted
  • 61. T G
    • Treatment options:
    • 1. Increasing dose of statin
    • 2. Add Fibrate (Finofibrate is preferable)
    • 3. Add Nicotinic acid
  • 62. Fibrates
    • Mechanism of action
      • Inhibition of cholesterol synthesis
      • Decreased TG synthesis
      • Inhibition of lipolysis in adipose tissue
      • Decreased production of VLDL /  clearance
      • Increased plasma and hepatic LPL activity
    • Effect on lipids
      •  TC,  LDL,  HDL,  TG
  • 63. Fibrates - Dosing and Precautions
    • Dosing
      • Gemfibrozil: 600mg BID
      • Micronized Fenofibrate: 67mg QD;  to 67-201mg QD
      • Clofibrate: 2g daily in divided doses
    • Adverse effects
      • Nausea, diarrhea, cholelithiasis, phototoxicity
    • Drug interactions
      • Increased risk of hepatotoxicity and/or myalgias with concurrent statins and/or niacin
      • Protein binding displacement (e.g., warfarin)
  • 64. 3 rd Goal
    • Low HDL-C (<40 mg/dL) is considered a tertiary goal
  • 65. Major causes of Low HDL
    • Heredity (40% to 60%)
    • Elevated triglycerides
    • Physical inactivity
    • Cigarette smoking
    • Diets rich in refined carbohydrates & trans – fats
    • Certain B.P. medication (diuretics – B blockers)
  • 66. Life style factors that Raise HDL
    • Physical activity
    • Weight loss
    • Diet high in mono unsaturated fats eg. Lean meat, Avocado, nuts, olive oil
    • Fish oil containing omega – 3 fatty acids
    • Smoking cessation
    • Small amounts of alcohol
  • 67. Medication that Raise HDL
    • Niacin
    • Statins
    • FIbrates
    • Estrogen for women
    • Alpha blockers
    • CETP inhibitor
    • HDL mimetic or artificial HDL
    • APO A Milano
  • 68. Common medications that increases levels of HDL and its subclasses Medication HDL HDL2 HDL3 Apo AI Statins +5 to 10% +5 + 30% -5 to +5% -5 to +5% Fibrates +10 to 15% -5% +5 to +30 -5 to +5 Niacin +25 to 50% +50 to 200% -5 to +5% +5 to +30%
  • 69. HDL
    • Niacin is drug of choice
    • It raises blood glucose level, but still can be used in diabetics with good control
  • 70. Niacin
    • Mechanism of action
      • Inhibition of free fatty acid release from adipose tissue
      • Inhibition of cAMP accumulation
      • Inhibition of VLDL and LDL synthesis
      • Increased LPL activity
    • Effects on lipids
      •  TC,  LDL,  HDL,  TG
      • Conversion of LDL phenotypic pattern B into pattern A
      • Lowers Lp(a)
  • 71. Niacin - Dosing
    • Immediate release
      • 100mg TID;  by 100mg TID every week as tolerated
      • Goal = 500-1000mg TID
    • Sustained release
      • 375mg QD;  gradually as needed
      • Goal = 500-2000mg QD
  • 72. Niacin - Precautions
    • Adverse effects
      • Flushing, pruritis, headache, fatigue (PG-mediated? -- ASA)
      • Gastritis, abdominal pain, aggravation of PUD, hepatotoxicity
      • Impaired glucose control,  uric acid concentrations
    • Drug interactions
      • Alcohol:  risk of hepatotoxicity
      • Statins, fibrates:  risk of hepatotoxicity and/or myalgias
      • Contra-Indication – H/o gout,peptic ulcer ds., liver ds.
  • 73. Other Drugs
    • Gastrointestinal-active medication such as a bile acid–binding sequestrant (the
    • resins cholestyramine and colestipol, or colesevelam, a nonabsorbable polymer)
    • Cholesterol-absorption inhibitor (e.g., ezetimibe)
  • 74. Bile Acid Sequestrants 1.) LDL Uptake Cholesterol 2.) Synthesis HMG CoA Bile Acids Cholesterol HMG CoA Bile Acids Intestines Intestines
  • 75. Bile Acid Sequestrants
    • Drug Dose Range
    • Cholestyramine 4–16 g
    • Colestipol 5–20 g
    • Colesevelam 2.6–3.8 g
  • 76. Ezetimibe
    • Ezetimibe is a cholesterol-absorption inhibitor.
    • It lowers LDL-C by about 20%, lowers TGs, and raises HDL-C slightly.
    • 10 mg/day, and it can be taken at any time of the day.
  • 77. Ezetimibe: A New Cholesterol Absorption Inhibitor
    • First of a new class of drugs with unique mechanism of action
      • Targets intestinal absorption of dietary and biliary cholesterol
      • Inhibits absorption of dietary and biliary cholesterol
      • Reduces plasma LDL-C
    Adapted from Leitersdorf E Eur Heart J Suppl 2001;3(suppl E):E17-E23; Miettinen TA Int J Clin Pract 2001;55:710-716; Stein E Eur Heart J Suppl 2001;3(suppl E):E11-E16.
    • In co-administration therapy with statins
      • Inhibits cholesterol absorption in the intestine and biosynthesis in the liver (dual inhibition)
      • Achieves lipid reductions greater than those with statins alone
  • 78.
    • Is useful as monotherapy for patients intolerant or nonresponsive to statins or enhanced benefits in addition to statins
    • Favorable safety and tolerability profile shown in clinical trials
      • similar to placebo
      • similar to statin alone, in coadministration
  • 79. Omega 3 fatty acids
    • The AHA recommends 2 to 4 g/day of eicosapentaenoic acid plus docosahexaenoic acid
  • 80. Herbs/Natural Products
    • Garlic
    • Fish Oils
    • Red Yeast Rice
    • Dietary Fiber
    • Oat Bran
    • Plant Sterols
    • Guggul
    • CoEnzyme Q10